PL235603B1 - Application of phospholipide preparation from egg yolks - Google Patents
Application of phospholipide preparation from egg yolks Download PDFInfo
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- PL235603B1 PL235603B1 PL408304A PL40830414A PL235603B1 PL 235603 B1 PL235603 B1 PL 235603B1 PL 408304 A PL408304 A PL 408304A PL 40830414 A PL40830414 A PL 40830414A PL 235603 B1 PL235603 B1 PL 235603B1
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- preparation
- antioxidant
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- oxidative stress
- lecithin
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Abstract
Wynalazek dotyczy zastosowania preparatu fosfolipidowego z żółtka jaj - super lecytyny do wytwarzania leku lub jako substancja czynna leku o działaniu antyoksydacyjnym do stosowania przy leczeniu chorób albo wspomagająco w terapii chorób o podłożu zapalnym. Rozwiązanie dotyczy również zastosowania super lecytyny jako środka farmaceutycznego, suplementu diety, dodatku żywieniowy lub jako składnika preparatów złożonych do stosowania przeciw wolnym rodnikom lub jako przeciwutleniacza.The invention concerns the use of a phospholipid preparation from egg yolk - super lecithin for the production of a medicine or as an active substance in a medicine with an antioxidant effect for use in the treatment of diseases or as an adjunct in the treatment of inflammatory diseases. The solution also applies to the use of super lecithin as a pharmaceutical, dietary supplement, nutritional supplement or as an ingredient of complex preparations for use against free radicals or as an antioxidant.
Description
Opis wynalazkuDescription of the invention
Przedmiotem wynalazku jest zastosowanie preparatu fosfolipidowego z żółtka jaj - super lecytyny, ujawnionego w opisie patentowym P.399338.The subject of the invention is the use of a phospholipid preparation from egg yolk - super lecithin, disclosed in patent description P.399338.
Reakcje utleniania i redukcji odgrywają niezwykle istotną rolę w regulacji procesów takich jak reakcje enzymatyczne, procesy metaboliczne oraz sygnalizacja międzykomórkowa. Obecność utleniaczy i biologicznych reduktorów w systemach wewnątrzkomórkowych jest niezbędna do zachowania nie tylko równowagi oksydoredukcyjnej, ale również zapewnienia prawidłowego funkcjonowania komórki. Zaburzenie tej równowagi z przewagą występowania czynników silnie utleniających powoduje tzw. stres oksydacyjny. Efektem stresu oksydacyjnego jest narażenie komórek na działanie reaktywnych form tlenu (ROS; reactive oxygen species) (Bartosz G. Druga twarz tlenu. Wydawnictwo Naukowe PWN Warszawa 1995).Oxidation and reduction reactions play an extremely important role in the regulation of processes such as enzymatic reactions, metabolic processes and intercellular signaling. The presence of oxidants and biological reducers in intracellular systems is necessary to maintain not only the oxidation-reduction balance, but also to ensure the proper functioning of the cell. Disturbance of this balance with the predominance of strongly oxidizing factors causes the so-called Oxidative stress. The effect of oxidative stress is the exposure of cells to reactive oxygen species (ROS) (Bartosz G. The second face of oxygen. Wydawnictwo Naukowe PWN Warszawa 1995).
Liczne badania kliniczne i doświadczalne nad stresem oksydacyjnym dowodzą, że nadprodukcja ROS towarzyszy wielu zmianom patologicznym takim jak nadciśnienie tętnicze, miażdżyca, choroba wieńcowa, choroba Alzheimera, stwardnienie rozsiane, cukrzyca typu II oraz choroby nowotworowe. Szacuje się, że stres oksydacyjny jest nieodłącznym elementem ponad stu chorób (Kołodziejczyk J. 3-nitrotyrozyna - marker stresu oksydacyjnego in vitro i in vivo. Diagnostyka Laboratoryjna 2010; 46(2): 141-145). Stres oksydacyjny w komórkach powoduje między innymi zaburzenie organizacji cytoszkieletu, zahamowanie syntezy NAD+, NADP+, uszkodzenie DNA, peroksydację lipidów oraz zaburzenie funkcji fizjologicznej niektórych białek, w tym upośledzenie zdolności katalitycznej enzymów lub ich inaktywację. Peroksydacja tłuszczu w ścianach naczyń przyczynia się do zmiany morfologii błon, które stają się sztywne, przepuszczalne dla jonów oraz bardziej wrażliwe na uszkodzenia (Karasek M., Lewiński A., Reiter R.J. Melatonina: znaczenie kliniczne i zastosowanie terapeutyczne. Endokrynologia Polska. 2001; 52:81-100). Aktywne rodniki w układzie krążenia upośledzają funkcję śródbłonka, wzmagają stan zapalny, zaburzają hemostazę, wpływają na aktywność enzymów, zaburzają równowagę między procesami prokoagulacyjnymi oraz antykoagulacyjnymi.Numerous clinical and experimental studies on oxidative stress prove that overproduction of ROS accompanies many pathological changes such as hypertension, atherosclerosis, coronary heart disease, Alzheimer's disease, multiple sclerosis, type II diabetes and cancer. It is estimated that oxidative stress is an inherent element of over a hundred diseases (Kołodziejczyk J. 3-nitrotyrosine - a marker of oxidative stress in vitro and in vivo. Diagnostyka Laboratoryjna 2010; 46(2): 141-145). Oxidative stress in cells causes, among others, disruption of the organization of the cytoskeleton, inhibition of NAD+ and NADP+ synthesis, DNA damage, lipid peroxidation and disruption of the physiological function of some proteins, including impairment of the catalytic ability of enzymes or their inactivation. Fat peroxidation in the vessel walls contributes to a change in the morphology of membranes, which become stiff, permeable to ions and more sensitive to damage (Karasek M., Lewiński A., Reiter R.J. Melatonin: clinical significance and therapeutic use. Endokrynologia Polska. 2001; 52 :81-100). Active radicals in the circulatory system impair the function of the endothelium, increase inflammation, disturb hemostasis, affect enzyme activity, and disturb the balance between procoagulant and anticoagulant processes.
Stres oksydacyjny odgrywa bardzo ważną rolę w chorobach układu krążenia. Podstawowym mechanizmem w patologii nadciśnienia tętniczego oraz zaburzenia funkcji śródbłonka przez ROS jest ograniczenie biodostępności tlenku azotu (NO) jednego z najważniejszych czynników naczynio-rozkurczających. NO z udziałem ROS przekształcany jest do anionu nadtlenoazotynowego (ONOO-), wykazującego działanie naczyniokurczące i prozakrzepowe (Rubanyi G.M., Vanhoutte P M. Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor. Am. J. Physiol. 1986; 250: 822-827). Równie istotne w patologii wielu chorób w tym chorób układu krążenia jest nitrowanie reszt tyrozynowych w łańcuchu polipeptydowym białek. Nitrowanie tyrozyny powoduje zmianę struktury białka, czego konsekwencją jest upośledzenie lub utrata funkcji fizjologicznej peptydu. Proces nitrowania tyrozyny związany jest ze wzrostem stężenia nadtlenoazotynów (ONOO-), w obecności których reszty tyrozyny przyjmują postać rodnika tyrozylowego, który reagując z dwutlenkiem azotu (NO2-) tworzy 3-nitrotyrozynę. Rodnik tyrozylowy może również ulec dimeryzacji tworząc 3,3’-dwutyrozynę, czego konsekwencją jest powstanie wiązań krzyżowych modyfikujących strukturę białek. Nitrotyrozynę powszechnie uznaje się za marker zmian zachodzących w wyniku działania reaktywnych form tlenu (Bian K., Ke Y., Kamisaki Y., Murad F. Proteomic Modification by Nitric Oxide. J. Pharmacol. Sci. 2006; 101:271-279; Radi R. Nitric oxide, oxidants, and protein tyrosine nitration. Proc. Natl. Acad. Sci USA. 2004; 101(12):4003-4008; Kołodziejczyk J. 3-nitrotyrozyna - marker stresu oksydacyjnego in vitro i in vivo; Diagnostyka Laboratoryjna 2010; 46(2): 141-145).Oxidative stress plays a very important role in cardiovascular diseases. The basic mechanism in the pathology of hypertension and impaired endothelial function due to ROS is the limitation of the bioavailability of nitric oxide (NO), one of the most important vasodilator factors. NO with the participation of ROS is transformed into peroxynitrite anion (ONOO - ), which has vasoconstrictive and prothrombotic properties (Rubanyi GM, Vanhoutte P M. Superoxide anions and hyperoxia inactivate relaxing endothelium-derived factor. Am. J. Physiol. 1986; 250: 822- 827). Equally important in the pathology of many diseases, including cardiovascular diseases, is the nitration of tyrosine residues in the polypeptide chain of proteins. Tyrosine nitration causes a change in the structure of the protein, resulting in impairment or loss of the physiological function of the peptide. The tyrosine nitration process is associated with an increase in the concentration of peroxynitrites (ONOO - ), in the presence of which tyrosine residues take the form of a tyrosyl radical, which reacts with nitrogen dioxide (NO2 - ) to form 3-nitrotyrosine. The tyrosyl radical can also dimerize to form 3,3'-dityrosine, which results in the formation of cross-links that modify the structure of proteins. Nitrotyrosine is widely considered to be a marker of changes occurring as a result of the action of reactive oxygen species (Bian K., Ke Y., Kamisaki Y., Murad F. Proteomic Modification by Nitric Oxide. J. Pharmacol. Sci. 2006; 101:271-279; Radi R. Nitric oxide, oxidants, and protein tyrosine nitration. Proc. Sci USA; Laboratory 2010; 46(2): 141-145).
Istotną rolę w redukcji stresu oksydacyjnego odgrywają tzw. antyoksydanty - czynniki, które w wyniku reakcji z ROS neutralizują je całkowicie lub częściowo (do formy mniej reaktywnej). W ostatnich latach podkreśla się znaczenie produktów o charakterze przeciwutleniającym w diecie. Dieta bogata w antyoksydanty może znaleźć zastosowanie zarówno w profilaktyce wielu chorób, jak również stanowić uzupełnienie standardowych terapii medycznych. Naturalnymi przeciwutleniaczami zawartymi w wielu produktach spożywczych są witaminy (A, B, C, D, E), selen, polifenole oraz fosfolipidy, w tym wielonienasycone kwasy tłuszczowe PUFA (polyunsaturated fatty acids) (Myung Seung-Kwon. Efficacy of vitamin and antioxidant supplements in prevention of cardiovascular disease: systematic review and meta-analysis of randomised controlled trials. BMJ 2013; 18:346). Jednak PUFA przypisuje się także niekorzystny udział w peroksydacji lipidów w patologii stresu oksydacyjnego. Związane jest to z obecnością nienasyconych wiązań podwójnych między atomami węgla w łańcuchach fosfolipidów, któreAn important role in reducing oxidative stress is played by the so-called antioxidants - factors that, as a result of reaction with ROS, neutralize them completely or partially (to a less reactive form). In recent years, the importance of antioxidant products in the diet has been emphasized. A diet rich in antioxidants can be used both in the prevention of many diseases and as a complement to standard medical therapies. Natural antioxidants contained in many food products are vitamins (A, B, C, D, E), selenium, polyphenols and phospholipids, including polyunsaturated fatty acids PUFA (polyunsaturated fatty acids) (Myung Seung-Kwon. Efficacy of vitamin and antioxidant supplements in prevention of cardiovascular disease: systematic review and meta-analysis of randomized controlled trials. BMJ 18:346). However, PUFAs are also attributed to an unfavorable role in lipid peroxidation in the pathology of oxidative stress. This is related to the presence of unsaturated double bonds between carbon atoms in phospholipid chains, which
PL 235 603 B1 z chemicznego punktu widzenia są reaktywne i łatwo ulegają reakcji z ROS, tworząc niestabilne, rodnikowe formy lipidowe. Efekt ten jest niezwykle znamienny dla centralnego układu nerwowego, którego budowa opiera się głównie na DHA (kwas dokozaheksaenowy) (Nowak J.Z. Oxidative stress, polyunsaturated fatty acids-derived oxidation products and bisretinoids as potential inducers of CNS diseases: focus on agerelated macular degeneration. Pharmacol. Rep. 2013; 65(2):288-304). Z kolei inne doniesienia wskazują na korzystną rolę PUFA z grupy omega-3 w redukcji stresu oksydacyjnego (Mori T.A., Puddey I.B., Burke V., Croft K.D., Dunstan D.W., Rivera J.H., Beilin L.J. Effect of omega 3 fatty acids on oxidative stress in humans: GC-MS measurement of urinary F2-isoprostane excretion. Redox Rep. 2000; 5(1):45-46; Mori T.A., Woodman R.J., Burke V., Puddey I.B., Croft K.D., Beilin L.J. Effect of eicosapentaenoic acid and docosahexaenoic acid on oxidative stress and inflammatory markers in treated-hypertensive type 2 diabetic subjects. Free Radic. Biol. Med. 2003; 35(7):772-781). Badania na gryzoniach dowodzą, że PUFA pochodzące z ryb wpływają na wzrost aktywności takich enzymów antyoksydacyjnych jak: katalaza (CAT), dysmutaza ponadtlenkowa (SOD) oraz peroksydaza glutationowa (GPX). Można zatem przypuszczać, że przeciwutleniające działanie PUFA jest związane z regulacją aktywności enzymów antyoksydacyjnych (Jahangiri A., Leifert W.R., Kind K.L., McMurchie E.J. Dietary fish oil alters cardiomyocyte Ca2+ dynamics and antioxidant status. Free Radic. Biol. Med. 2006; 40(9): 1592-15602; Rahman M., Halade G.V., Bhattacharya A., Fernandes G. The fat-1 transgene in mice increases antioxidant potential, reduces pro-inflammatory cytokine levels, and enhances PPAR-gamma and SIRT-1 expression on a calorie restricted diet. Oxid. Med. Cell Longev. 2009; 2(5):307-316; Chandrasekar B., Fernandes G. Decreased pro-inflammatory cytokines and increased antioxidant enzyme gene expression by ω-3 lipids in murine lupus nephritis. Biochem. Biophys. Res. Commun. 1994; 200:893-898; Venkatraman J.T., Chandrasekar B., Kim J.D. Fernandes, G. Effects of n-3 and n-6 fatty acids on the activities and expression of hepatic antioxidant enzymes in autoimmune-prone NZB x NZW F1 mice. Lipids. 1994; 29:561-568).PL 235 603 B1 are reactive from a chemical point of view and easily react with ROS, creating unstable, radical lipid species. This effect is extremely significant for the central nervous system, the structure of which is based mainly on DHA (docosahexaenoic acid) (Nowak J.Z. Oxidative stress, polyunsaturated fatty acids-derived oxidation products and bisretinoids as potential inducers of CNS diseases: focus on agerelated macular degeneration. Pharmacol .Rep. 2013; 65(2):288-304). In turn, other reports indicate a beneficial role of omega-3 PUFAs in reducing oxidative stress (Mori T.A., Puddey I.B., Burke V., Croft K.D., Dunstan D.W., Rivera J.H., Beilin L.J. Effect of omega 3 fatty acids on oxidative stress in humans: GC-MS measurement of urinary F2-isoprostane excretion. Redox Rep. 5(1):45-46; docosahexaenoic acid on oxidative stress and inflammatory markers in treated-hypertensive type 2 diabetic subjects. Biol. 2003; Studies on rodents prove that PUFAs from fish increase the activity of such antioxidant enzymes as: catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX). It can therefore be assumed that the antioxidant effect of PUFA is related to the regulation of the activity of antioxidant enzymes (Jahangiri A., Leifert W.R., Kind K.L., McMurchie E.J. Dietary fish oil alters cardiomyocyte Ca2+ dynamics and antioxidant status. Free Radic. Biol. Med. 2006; 40( 9): 1592-15602; Rahman M., Halade G.V., Bhattacharya A., Fernandes G. The fat-1 transgene in mice increases antioxidant potential, reduces pro-inflammatory cytokine levels, and enhances PPAR-gamma and SIRT-1 expression a calorie restricted diet. Med. Cell Longev. 2(5): 307-316; Chandrasekar B. Decreased pro-inflammatory cytokines and increased antioxidant enzyme gene expression . Biochem. Biophys. Commun. 1994; Venkatraman J., Kim J. D. Effects of n-3 and n-6 fatty acids in autoimmune-prone NZB x NZW F1 mice. 1994;
Wiadomo również, że DHA (kwas dokozaheksaenowy) i EPA (kwas eikozapentaenowy) redukuje stres oksydacyjny przez zahamowanie ekspresji oksydazy NADPH (nicotinamide adenine dinucleotide phosphate-oxidase) - enzymu odpowiedzialnego za produkcje ROS (Depner C.M., Philbrick K.A., Jump D.B. Docosahexaenoic acid attenuates hepatic inflammation, oxidative stress, and fibrosis without decreasing hepatosteatosis in a Ldlr(-/-) mouse model of western diet-induced nonalcoholic steatohepatitis. J. Nutr. 2013; 143(3):315-323; Massaro M., Habib A., Lubrano L, Del Turco S., Lazzerini G., Bourcier T., Weksler B.B., De Caterina R. The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition. Proc. Natl. Acad. Sci. USA. 2006; 103(41): 15184-15189). U szczurów ze spontanicznym nadciśnieniem - SHR - dieta wzbogacona w polifenole (przez dodanie 1% fasoli azuki - czerwona soja) obniża poziom stresu oksydacyjnego w aorcie (Mukai Y., Sato S. Polyphenol-containing azuki bean (Vigna angularis) seed coats attenuate vascular oxidative stress and inflammation in spontaneously hypertensive rats. J. Nutr. Biochem. 2011; 22(1):16-21). Znane jest również działanie antyoksydacyjne fosfatydylocholiny w przebiegu nadciśnienia (Eshiginia S., Gapparov M.M., Soto Kh. Influence of phospholipids on efficiency of dietary therapy and parameters of lipids metabolism in patients with hypertension). Vopr. Pitan. 2005;74(5):28-31).It is also known that DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) reduce oxidative stress by inhibiting the expression of NADPH oxidase (nicotinamide adenine dinucleotide phosphate-oxidase) - the enzyme responsible for the production of ROS (Depner C.M., Philbrick K.A., Jump D.B. Docosahexaenoic acid attenuates hepatic acid). inflammation, oxidative stress, and fibrosis without decreasing hepatosteatosis in a Ldlr(-/-) mouse model of western diet-induced nonalcoholic steatohepatitis. 2013; , Lubrano L, Del Turco S., Lazzerini G., Bourcier T., Weksler B.B., De Caterina R. The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition Proc Natl Sci USA 2006; In rats with spontaneous hypertension - SHR - a diet enriched with polyphenols (by adding 1% azuki bean - red soybean) reduces the level of oxidative stress in the aorta (Mukai Y., Sato S. Polyphenol-containing azuki bean (Vigna angularis) seed coats attenuate vascular oxidative stress and inflammation in spontaneously hypertensive rats. J. Nutr. 2011; The antioxidant effect of phosphatidylcholine in the course of hypertension is also known (Eshiginia S., Gapparov M.M., Soto Kh. Influence of phospholipids on efficiency of dietary therapy and parameters of lipids metabolism in patients with hypertension). Vopr. Pitan. 2005;74(5):28-31).
Istotą wynalazku jest preparat fosfolipidowy otrzymany sposobem ujawnionym w opisie patentowym PL218452, zwany super lecytyną, do zastosowania do wytwarzania leku lub jako substancja czynna leku o działaniu antyoksydacyjnym, przy leczeniu chorób albo wspomagająco w terapii chorób o podłożu zapalnym, zwłaszcza chorób nowotworowych (ICD10: C.00.0 do D.48), otyłości (ICD10: E.66.0), cukrzycy (ICD10 E.10.0 do E.14.9), miażdżycy (ICD10 I.70.9).The essence of the invention is a phospholipid preparation obtained by the method disclosed in patent description PL218452, called super lecithin, for use in the production of medicines or as an active substance in a medicine with an antioxidant effect, in the treatment of diseases or as an adjunct in the treatment of inflammatory diseases, especially cancer (ICD10: C .00.0 to D.48), obesity (ICD10: E.66.0), diabetes (ICD10 E.10.0 to E.14.9), atherosclerosis (ICD10 I.70.9).
Istotą wynalazku jest także zastosowanie preparatu fosfolipidowego otrzymanego sposobem ujawnionym w opisie patentowym PL218452, zwanego super lecytyną, jako suplement diety, dodatek żywieniowy lub jako składnik preparatów złożonych, do stosowania przeciw wolnym rodnikom lub jako przeciwutleniacz.The essence of the invention is also the use of a phospholipid preparation obtained by the method disclosed in patent description PL218452, called super lecithin, as a dietary supplement, nutritional additive or as an ingredient of complex preparations, for use against free radicals or as an antioxidant.
Przedstawione poniżej wyniki wskazują na wyraźne działanie przeciwutleniające preparatu fosfolipidowego z jaj kurzych, przejawiające się obniżeniem poziomu nitrotyrozyny w surowicy krwi badanych zwierząt. Działanie antyoksydacyjne badanego preparatu jest niezależne od efektu hipotensyjnego, bowiem obniżenie poziomu nitrotyrozyny obserwowane jest zarówno u szczurów z nadciśnieniem (SHR-Spontanously Hypertensive Rats), jak i zdrowych (WKY - Wistar Kyoto Rats).The results presented below indicate a clear antioxidant effect of the phospholipid preparation from chicken eggs, manifested by a reduction in the level of nitrotyrosine in the blood serum of the tested animals. The antioxidant effect of the tested preparation is independent of the hypotensive effect, because a reduction in nitrotyrosine levels is observed in both hypertensive rats (SHR - Spontaneously Hypertensive Rats) and healthy rats (WKY - Wistar Kyoto Rats).
P r z y k ł a d. W doświadczeniu wykorzystano siedmiotygodniowe samce szczurów z nadciśnieniem SHR/NCrl (Spontanously Hypertensive Rats; Charles River), oraz samce zdrowych szczurówExample: Seven-week-old male SHR/NCrl hypertensive rats (Spontaneously Hypertensive Rats; Charles River) and healthy male rats were used in the experiment.
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WKY/NCrl (Wistar Kyoto Rats; szczep referencyjny dla SHR). Na realizację badań uzyskano zgodę Lokalnej Komisji Bioetycznej we Wrocławiu w dniu 15.12.2010 r., numer 61/2010. W doświadczeniu użyto paszę ubogą w wielonienasycone kwasy tłuszczowe (Labofeed B uboga w PUFA, Kcynia, Polska), wykluczając tym samym wpływ PUFA pochodzących z paszy. Dostęp szczurów do paszy i wody był nieograniczony. Zwierzęta podzielono na cztery grupy: dwie doświadczalne i dwie kontrolne.WKY/NCrl (Wistar Kyoto Rats; reference strain for SHR). The consent to carry out the research was obtained from the Local Bioethics Committee in Wrocław on December 15, 2010, number 61/2010. The experiment used feed low in polyunsaturated fatty acids (Labofeed B low in PUFA, Kcynia, Poland), thus excluding the influence of PUFA from the feed. Rats had unlimited access to feed and water. The animals were divided into four groups: two experimental and two control.
Grupy doświadczalne (LP) stanowiły:The experimental groups (LP) were:
• grupa SHR otrzymująca preparat fosfolipidowy z żółtek jaj, zwany super lecytyną, opisany w zgłoszeniu patentowym P.399338, razem z paszą ubogą (SHR/LP; ni = 15), • grupa WKY otrzymująca tenże preparat razem z paszą ubogą (WKY/LP; n2 = 11).• SHR group receiving a phospholipid preparation from egg yolks, called super lecithin, described in patent application P.399338, together with lean feed (SHR/LP; ni = 15), • WKY group receiving this preparation together with lean feed (WKY/LP ; n2 = 11).
Grupy kontrolne (K) stanowiły:Control groups (K) consisted of:
• grupa SHR otrzymująca tylko paszę ubogą w PUFA (SHR/K; ns = 15), • grupa WKY otrzymująca tylko paszę ubogą w PUFA (WKY/K; m = 11), • przy czym n, to liczba osobników w danej grupie.• SHR group receiving only feed low in PUFA (SHR/K; ns = 15), • WKY group receiving only feed low in PUFA (WKY/K; m = 11), • where n is the number of individuals in a given group.
Średnie dzienne spożycie preparatu w grupach doświadczalnych wynosiło 1,5 g/osobnika. Tym samym dieta grup wzbogaconych preparatem fosfolipidowym z jaj zawierała 5% fosfatydylocholiny; 0,65% kwasów omega-3 oraz 0,95% omega-6. W Tabeli 1 przedstawiono skład preparatu.The average daily intake of the preparation in the experimental groups was 1.5 g/individual. Thus, the diet of the groups enriched with the egg phospholipid preparation contained 5% phosphatidylcholine; 0.65% omega-3 and 0.95% omega-6 acids. Table 1 shows the composition of the preparation.
Tabela 1. Procentowy skład kwasów tłuszczowych we frakcji fosfolipidowej z żółtka jaja kurzego.Table 1. Percentage of fatty acids in the phospholipid fraction from egg yolk.
Fosfolipidy z jaj podawano przez dwanaście tygodni, po tym czasie wykonano badanie sekcyjne i zabezpieczono materiał do dalszych badań. W surowicy krwi oznaczono poziom nitrotyrozyny przy użyciu testu immunoenzymatycznego ELISA (zestaw Nitrotyrosine ELISA; nr 17-376, Merck, MA, USA).Phospholipids from eggs were administered for twelve weeks, after which an autopsy was performed and the material was secured for further research. The level of nitrotyrosine in blood serum was determined using an enzyme-linked immunosorbent assay (ELISA) (Nitrotyrosine ELISA kit; no. 17-376, Merck, MA, USA).
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Analizę wykonano zgodnie z instrukcją dołączoną do zestawu. Wyniki dla wszystkich grup szczurów SHR i WKY podsumowano w tabeli 2 oraz na wykresie 1.The analysis was performed in accordance with the instructions included with the kit. The results for all groups of SHR and WKY rats are summarized in Table 2 and Figure 1.
Tabela 2. Poziom nitrotyrozyny [pg/ml] w surowicy krwi dla każdego osobnika z grup: SHR/K, SHR/LP oraz wartości średnie i odchylenie standardowe dla każdej grupyTable 2. Level of nitrotyrosine [pg/ml] in blood serum for each individual from the groups: SHR/K, SHR/LP and mean values and standard deviation for each group
Wykres 1. Średnie stężenie nitrotyrozyny [pg/ml] w surowicy krwi szczurów SHR oraz WKY z grup kontrolnych (K) i doświadczalnych (LP).Graph 1. Average concentration of nitrotyrosine [pg/ml] in the blood serum of SHR and WKY rats from control (K) and experimental (LP) groups.
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Preparat fosfolipidowy z nowej generacji jaj wykazuje działanie antyoksydacyjne obniżając poziom nitrotyrozyny w surowicy krwi zarówno u szczurów z nadciśnieniem (SHR), jak i zdrowych (WKY). Poziom nitrotyrozyny w surowicy krwi grupy SHR otrzymującej preparat (SHR/LP) jest o 34% niższy niż w grupie SHR kontrolnej (SHR/K). U szczurów WKY natomiast, fosfolipidy z nowej generacji jaj, obniżają stężenie nitrotyrozyny o 30% w porównaniu do grupy kontrolnej (WKY/LP vs. WKY/K).A phospholipid preparation from a new generation of eggs has an antioxidant effect by reducing the level of nitrotyrosine in blood serum in both hypertensive (SHR) and healthy (WKY) rats. The level of nitrotyrosine in the blood serum of the SHR group receiving the preparation (SHR/LP) is 34% lower than in the SHR control group (SHR/K). In WKY rats, however, phospholipids from a new generation of eggs reduce nitrotyrosine concentration by 30% compared to the control group (WKY/LP vs. WKY/K).
W grupach doświadczalnych (LP) obu badanych szczepów szczurów obserwuje się podobny procentowy spadek poziomu badanego markera stresu oksydacyjnego (nitrotyrozyny) w surowicy krwi (Test U Manna-Whitneya, p<0,05).In the experimental groups (LP) of both tested strains of rats, a similar percentage decrease in the level of the tested oxidative stress marker (nitrotyrosine) in blood serum is observed (Mann-Whitney U test, p<0.05).
Powyższe wyniki dowodzą, że preparat fosfolipidowy, pochodzący od kur projektowanych a ujawniony w opisie patentowym P.399338, obniża poziom stresu oksydacyjnego. Działanie przeciwutleniające powszechnie uznaje się za korzystne w prewencji oraz terapii wielu chorób. Biorąc pod uwagę stan techniki można przypuszczać, że potencjał antyoksydacyjny preparatu może być związany z obecnością fosfatydylocholiny oraz PUFA z grupy omega-3 (w tym DHA i EPA). Nie można ponadto wykluczyć wpływu innych składników preparatu takich jak niska wartość proporcji kwasów omega-6 do omega-3. Z pewnością korzystny wpływ preparatu fosfolipidowego w patologii stresu oksydacyjnego warunkuje jego złożoność i każdy z elementów składowych może odgrywać częściową rolę w ogólnym efekcie przeciwutleniającym.The above results prove that the phospholipid preparation, derived from engineered chickens and disclosed in patent description P.399338, reduces the level of oxidative stress. The antioxidant effect is widely recognized as beneficial in the prevention and treatment of many diseases. Taking into account the state of the art, it can be assumed that the antioxidant potential of the preparation may be related to the presence of phosphatidylcholine and omega-3 PUFA (including DHA and EPA). Moreover, the influence of other ingredients of the preparation cannot be ruled out, such as the low value of the ratio of omega-6 to omega-3 acids. Certainly, the beneficial effect of a phospholipid preparation in the pathology of oxidative stress determines its complexity and each of the components may play a partial role in the overall antioxidant effect.
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